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Multidimensional Coculture System to Model Lung Squamous Carcinoma Progression
Published on: March 17, 2020
MiR-125b-1-3p Exerts Antitumor Functions in Lung Carcinoma Cells by Targeting S1PR1
Xiang Zhang1, Yu Liu1, Wei-Cong Huang1
1Department of Thoracic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China.
Background:
MicroRNAs (miRNAs) have been extensively studied over the decades and have been identified as potential molecular targets for cancer therapy. To date, many miRNAs have been found participating in the tumorigenesis of non-small cell lung cancer (NSCLC). The present study was designed to evaluate the functions of miR-125b-1-3p in NSCLC cells.
Methods:
MiR-125b-1-3p expression was detected in tissue samples from 21 NSCLC patients and in NSCLC cell lines using the real-time polymerase chain reaction. A549 cell lines were transfected with a miR-125b-1-3p mimic or miR-125b-1-3p antisense. Cell counting kit-8, wound healing, Matrigel invasion assays, and flow cytometry were used to assess the effects of these transfections on cell growth, migration, invasion, and apoptosis, respectively. Western blotting was used to detect apoptosis-related proteins, expression of S1PR1, and the phosphorylation status of STAT3. Significant differences between groups were estimated using Student's t-test or a one-way analysis of variance.
Results:
MiR-125b-1-3p was downregulated in NSCLC samples and cell lines. Overexpression of miR-125b-1-3p inhibited NSCLC cell proliferation (37.8 ± 9.1%, t = 3.191, P = 0.013), migration (42.3 ± 6.7%, t = 6.321, P = 0.003), and invasion (57.6 ± 11.3%, t = 4.112, P = 0.001) and simultaneously induced more NSCLC cell apoptosis (2.76 ± 0.78 folds, t = 3.772, P = 0.001). MiR-125b-1-3p antisense resulted in completely opposite results. S1PR1 was found as the target gene of miR-125b-1-3p. Overexpression of miR-125b-1-3p inhibited S1PR1 protein expression (27.4 ± 6.1% of control, t = 4.083, P = 0.007). In addition, S1PR1 siRNA decreased STAT3 phosphorylation (16.4 ± 0.14% of control, t = 3.023, P = 0.015), as in cells overexpressing miR-125b-1-3p (16.7 ± 0.17% of control, t = 4.162, P = 0.026).
Conclusion:
Our results suggest that miR-125b-1-3p exerts antitumor functions in NSCLC cells by targeting S1PR1.
Insights
MicroRNA miR-125b-1-3p is downregulated in non-small cell lung cancer (NSCLC). Restoring its levels inhibits NSCLC cell growth, migration, and invasion, while promoting apoptosis by targeting S1PR1.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- MicroRNAs (miRNAs) are key regulators in cellular processes.
- Dysregulation of miRNAs is implicated in non-small cell lung cancer (NSCLC) tumorigenesis.
- MiR-125b-1-3p is a potential therapeutic target in NSCLC.
Purpose of the Study:
- To investigate the functional role of miR-125b-1-3p in NSCLC.
- To determine the molecular mechanisms underlying miR-125b-1-3p's action in NSCLC cells.
Main Methods:
- Real-time PCR for miR-125b-1-3p expression analysis in patient samples and cell lines.
- Transfection of NSCLC cells with miR-125b-1-3p mimic or antisense.
- Cell counting kit-8, wound healing, and Matrigel invasion assays to assess proliferation, migration, and invasion.
- Flow cytometry for apoptosis analysis.
- Western blotting to detect apoptosis-related proteins, S1PR1 expression, and STAT3 phosphorylation.
Main Results:
- MiR-125b-1-3p expression was significantly downregulated in NSCLC tissues and cell lines.
- Overexpression of miR-125b-1-3p suppressed NSCLC cell proliferation, migration, and invasion, and induced apoptosis.
- S1PR1 was identified as a direct target of miR-125b-1-3p, with its expression inhibited by miR-125b-1-3p.
- S1PR1 knockdown mimicked the effects of miR-125b-1-3p overexpression on STAT3 phosphorylation.
Conclusions:
- MiR-125b-1-3p exhibits significant antitumor functions in NSCLC.
- The antitumor effects of miR-125b-1-3p are mediated through the targeting of S1PR1.
- MiR-125b-1-3p represents a promising therapeutic candidate for NSCLC treatment.
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